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efflux
and increase in dark cell number in choroid plexus
epithelium
1 Program in Neurosurgery,
The cerebrospinal
fluid (CSF)-generating choroid plexus (CP) has many
V1 binding sites for arginine
vasopressin (AVP). AVP decreases CSF formation rate and choroidal blood
flow, but little is known about how AVP alters ion transport across the
blood-CSF barrier. Adult rat lateral ventricle CP was loaded with
36Cl
,
exposed to AVP for 20 min, and then placed in isotope-free artificial CSF to measure release of
36Cl
.
Effect of AVP at 10
12 to
10
7 M on the
Cl
efflux rate coefficient
(in s
1) was quantified.
Maximal inhibition (by 20%) of
Cl
extrusion at
10
9 M AVP was prevented by
the V1 receptor antagonist
[
-mercapto-
,
-cyclopentamethyleneproprionyl1,O-Me-Tyr2,Arg8]vasopressin.
AVP also increased by more than twofold the number of dark and possibly
dehydrated but otherwise morphologically normal choroid epithelial
cells in adult CP. The V1 receptor
antagonist prevented this AVP-induced increment in dark cell frequency.
In infant rats (1 wk) with incomplete CSF secretory ability,
10
9 M AVP altered neither
Cl
efflux nor dark cell
frequency. The ability of AVP to elicit functional and structural
changes in adult, but not infant, CP epithelium is discussed in regard
to ion transport, CSF secretion, intracranial pressure, and hydrocephalus.
cerebrospinal fluid homeostasis; chloride-36 efflux rate coefficient; hydrocephalus; V1 receptor antagonist; neuroendocrine regulation; arginine vasopressin
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